Effects of supplemental nanoparticle trivalent chromium on the nutrient utilization, growth performance and serum traits of broilers.

The aim of this study was to investigate the effect of dietary supplementation of nanoparticle trivalent chromium on nutrient utilization, growth performance and serum traits of broilers. This study included two trials. In trial 1, 32 three-week-old broilers were divided into four groups: the control, chromium chloride (CrCl3), chromium picolinate (CrPic) and nanoparticle chromium picolinate (NanoCrPic). Chromium was added at a 1200 µg/kg level to evaluate the nutrient and chromium utilization. In trial 2, 160 one-day-old broilers were randomly divided into four groups as in trial 1, with four replicates. The results of trial 1 indicated that the chromium utilization is as follows: NanoCrPic > CrPic > CrCl3 and control groups, with significant differences between groups (p < 0.05). Crude fat utilization in CrCl3 group was lower than in that the control group (p < 0.05). The results of trial 2 indicated that feed intake of 4-5 weeks showed better result in the CrCl3 group than that in the CrPic group (p < 0.05). The results of serum traits indicated that the LDL-cholesterol in the NanoCrPic groups was lower than that in the CrPic group (p < 0.05). The NanoCrpic and CrPic groups showed significantly increased serum chromium concentration when compared with the control and CrCl3 groups; the triglyceride level in the CrCl3 group was lower than that in the CrPic group (p < 0.05). This study concluded that compared with CrPic, NanoCrpic supplementation could increase chromium utilization and lower the serum LDL-cholesterol of broilers.

[Effect of reduqing on HL-60 cells in secreting tumor necrosis factor alpha production and on TNF alpha converting enzyme mRNA expression].

OBJECTIVE: To explore the molecular mechanism of inhibiting effects of Reduqing on the release of tumor necrosis factor alpha (TNF alpha). METHODS: Using cytobiologic and molecular biologic technique to observe the effects of Reduqing on HL-60 cells in producing inflammatory cytokine secreting TNF alpha (sTNF alpha) and on mRNA expression of TNF alpha converting enzyme (TACE). RESULTS: (1) Reduqing, diluted in ratio 1:30, could effectively inhibit the increased HL-60 production of sTNF-alpha induced by lipopolysaccharides (LPS); (2) Although no obvious effect on TACE was shown when Reduqing was applied alone on HL-60 cells, there was evident inhibitory effect of Reduqing on TACE mRNA expression enhancement induced by LPS. CONCLUSION: Reduqing could have the double inhibitory effects both on sTNF-alpha production and on the gene expression of its key enzyme, i.e. TACE stimulated by LPS, suggesting that it might be a hopeful and excellent natural TACE inhibitor.

American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth.

BACKGROUND AND OBJECTIVES: American ginseng (Panax quinquefolius L.) purportedly alleviates menopause symptoms because of putative estrogenicity. METHODS: Using a standardized American ginseng (AG) extract in MCF-7 breast cancer cells, the objectives were to evaluate the ability of AG to induce the estrogen- regulated gene pS2 by Northern blot analysis, determine the effect on cell growth using the MTT assay, and evaluate the cell cycle effects by flow cytometry. RESULTS: AG and estradiol equivalently induced RNA expression of pS2. AG, in contrast to estradiol, caused a dose-dependent decrease in cell proliferation (P < 0.005). AG had no adverse effect on the cell cycle while estradiol significantly increased the proliferative phase (percent S-phase) and decreased the resting phase (G(0)-G(1) phase) (P < 0.005). Concurrent use of AG and breast cancer therapeutic agents resulted in a significant (P < 0.005) suppression of cell growth for most drugs evaluated. CONCLUSIONS: In vitro use of AG and breast cancer therapeutics synergistically inhibited cancer cell growth.

[Effects of injectio reduqing on plasma IL-8 and nitric oxide levels in rabbits with endotoxin induced disseminated intravascular coagulation].

Experiments were performed for investigating the effects of Injectio Reduqing (RDQ) on plasma interleukin-8 (IL-8), NO2-/NO3-, complement 5a(C5a) and polymorphonuclear neutrophilic leukocyte (PMN) Chemotaxis Index (CI) in rabbits with endotoxin-induced disseminated intravascular coagulation (DIC). The results showed that plasma IL-8, NO2-/NO3-, C5a and CI levels of PMN increased markedly in model group, which were confirmed pathologically with obvious damage of tissues or organs. While in RDQ group the abov-mentioned parameters and damage of tissues or organs were reduced significantly (P < 0.01). The results suggested that the IL-8 and NO might be involved in pathogenesis of endotoxin-induced DIC, and RDQ could be used in preventing or treating DIC through mechanism of regulation of cytokines network.

[Effects of reducing injection on plasma TNF-alpha and IL-6 levels in rabbits with endotoxin-induced DIC].

Plasma TNF-a and IL-6 levels of endotoxin-induced DIC in rabbits were measured by ELISA methods. Simultaneously, the effects of Reduqing (RDQ) on TNF-alpha and IL-6 were also studied. The results showed that TNF-alpha and IL-6 levels increased markedly in model group, which were confirmed with obvious damage of tissue or organ. Co-administration of RDQ could reduce plasma TNF-alpha and IL-6 levels, together with mild tissue or organ damage. These results indicated TNF-alpha and IL-6 might be involved in pathogenesis of endotoxin-induced DIC, RDQ might be used in preventing or treating DIC through mechanism of reducing TNF-alpha and IL-6 levels.

[Study on objective parameters of syndrome differentiation of diabetic nephropathy].

This is a study about objective parameters of Syndrome Differentiation of diabetic nephropathy (DN) using radio immunoassay (RIA) technique. The result showed that beta 2-microglobulin (beta 2-mG), alpha 1-microglobulin (alpha 1-mG) in blood rose significantly in both groups. The group of Spleen-Kidney Deficiency and Qi-Blood Deficiency as well as the group of Yang Deficiency caused edema and upward gush of turbid Yin, there was significant difference between two groups, also there was significant difference between the two groups in measuring on atrial natriuretic factor (ANP), pancreatic glucagon (PG) in blood and beta 2-mG. Immunoglobulin G (IgG), albumin (Alb), secretory immunoglobulin A(SIg A) in urine. So above-mentioned parameters offered us some objective data on Syndrome Differentiation of DN. It is vital in guiding the Syndrome Differentiation and treatment of DN.

Effects of zaizhang-I, a traditional Chinese herbal medicine, on hematopoietic recovery from radiation injury in mice.

Effects of Zaizhang-I (ZZ-I) on the recovery of hemopoietic systems from radiation injury were investigated. Mice, irradiated with 6.0 Gy-rays, were injected i.p. once daily for 7 consecutive days with either ZZ-I or saline (0.01 ml/g body wt.). The experiments showed that ZZ-I significantly promoted the recovery of not only peripheral WBC, BMC, CFU-S and CFU-GM but also the abnormal femur micro-vessel system such as blood vessels and sinus ectasia, hyperemia and hemorrhage etc. These results suggest that ZZ-I could accelerate hemopoietic recovery from radiation injury in mice by stimulating hemopoietic stem cells and improving hemopoietic inductive microenvironment (HIM).

Effects of zaizhang-I, a traditional Chinese medicine, on immunologically mediated aplastic anemia in mice.

Immunologically mediated aplastic anemia in mice were used as animal models to study the the curative effect of Zaizhang-I in term of the changes of two pathogenetic aspects in aplastic mice, namely the deficiency of hematopoietic stem cells and the disturbance of immunology. Our results demonstrated that in aplastic mice, after treatment by Zaizhang-I, the loss of mature hematopoietic cells (WBC, RBC, Plt) were reduced, and marrow cellular cytosis, and their clinical findings were improved, indicating a partial remission. The present data show that its curative mechanism lies in the action of promoting the recovery of colony forming unit-spleen (CFU-S) and reversing immunologically-induced plasma colony forming unit granulocyte/macrophage (CFU-GM) inhibitory activity. Natural killer cells activity (Nka) and interleukin-2, tumor necrosis factors (TNF) were also so examined to further understand the mechanism by which Zaizhang-I reverse plasma hematopoietic activity.

[Antagonistic effect of re du qing on damage of hepatocytic microsomes in rabbits with endotoxin-induced disseminated intravascular coagulation].

In this study, the generalized Shwartzman reaction of rabbit induced by endotoxin of Escherichia Coli was built as DIC models. The experiment showed that the levels of lipid peroxide (LPO) in the hepatocytic microsomes of model group were increased significantly, whereas the cytochrome P-450 (Cyto. P-450) contents and aniline hydroxylase activities were obviously decreased. In the Re Du Qing (RDQ) group and dexamethasone group the decrease of LPO in hepatocytic microsomes as well as the reduction of Cyto. P-450 contents and aniline hydroxylase activities were alleviated. Furthermore, the correlation analysis indicated a significant negative correlation between levels of LPO in microsomes and the Cyto. P-450 contents as well as aniline hydroxylase activities. This study indicates the LPO may play an important role in the damage of hepatocytic microsomes and RDQ could prevent hepatocytic microsomes from injury of rabbits with endotoxin-induced DIC.

[Scavenging effect of re-du-qing on free radicals].

The general Shwartzman reactions of rabbits were induced by intravenously injecting endotoxin twice with 24 hours interval. The lipid peroxides (LPO) in sera and liver homogenates of rabbits in normal saline group (12.26 +/- 0.84 n mol MDA/ml, 1.86 +/- 0.43 n mol MDA/mg protein respectively) were significantly higher than those of rabbits in normal control group (7.93 +/- 2.90, 1.31 +/- 0.22, both P less than 0.01), and LPO in sera and liver homogenates of rabbits in Re-Du-Qing group (6.55 +/- 2.97, 1.19 +/- 0.12) were evidently lower than those of rabbits in normal saline group (P less than 0.01), accessed to the LPO level of rabbits in normal control group. In in vitro experiment, LPO of mitochondria in Re-Du-Qing group (1.50 +/- 0.43 n mol MDA/mg protein) dramatically decreased, compared with that of endotoxin group (2.39 +/- 0.69, P less than 0.05) and of control group (2.23 +/- 0.75, P less than 0.05). The findings of both in vivo and in vitro experiments showed that Re-Du-Qing possesses scavenging effect on free radicals. In view of the detoxification mechanism of Re-Du-Qing, in addition to inhibiting bacteria and degrading. endotoxin, the scavenging effect of Re-Du-Qing on free radicals are also included.

[Preventive effect of re du qing on hepatocytes and mitochondria damaged by lipid peroxidation in experimental rabbits with endotoxin-induced disseminated intravascular coagulation].

In this study, the general Shwartzman reaction of rabbits induced by Escherichia Coli endotoxin was made as DIC models. The experiments showed that the levels of lipid peroxide (LPO) in hepatic tissue and mitochondria in the model group were increased significantly compared with the control group (P less than 0.01), while superoxide dismutase (SOD) activity in hepatic tissue and glutathione peroxidase (GSH-Px) activity in hepatic tissue and mitochondria were decreased significantly (P less than 0.01). The levels of LPO in hepatic tissue and mitochondria in Re Du Qing (RDQ) group and vitamin E (VE) group were decreased significantly (P less than 0.01 and P less than 0.05 respectively) compared with the model group. The levels of LPO in the RDQ group did not differ from the control group (P greater than 0.05), but the levels of LPO in the VE group were still higher than those in the control group significantly (P less than 0.05). The SOD activity in hepatic tissue and GSH-Px activity in hepatic tissue and mitochondria in both RDQ group and VE group were also significantly higher than those in the model group (P less than 0.01). These data suggest that the levels of oxygen free radicals were increased in hepatocytes and mitochondria. This is related to the decreased activities of SOD and GSH-Px in the course of pathogenesis of endotoxin-induced DIC. This study indicates that lipid peroxidation might be one of the important mechanisms resulting in hepatocellular and mitochondria from oxidative damage.

[Experimental studies on the antagonistic effect of re du qing on endotoxin-induced damage of lysosomes and mitochondria].

A rabbit endotoxic DIC model was preliminarily performed. The structures of lysosomes and mitochondria in liver cells were evidently destroyed as observed under electronic microscope, whereas those rabbits pretreated with Re Du Qing (RDQ, formerly named anti-inflammatory No. 6)--a mixture of Chinese traditional herbs providing antipyretic and detoxifying action, showed principally normal ultrastructure in liver cells. In lysosomal functional studies, the activity of the lysosomal marker enzyme--acid phosphate (ACP) was 79.0 +/- 4.7% (M +/- SD) in model group, higher than pretreated group (54.01 +/- 4.0%, P less than 0.01). Studies on the mitochondrial function showed that the significant criteria of the respiratory activity of mitochondria--respiratory control ratios (RCR) was 2.83 +/- 1.08 in model group and markedly lower than pretreated group (5.46 +/- 1.25, P less than 0.01). Mitochondrial ATPase activity (mu mol pi/min/mg pr.) was lower in model group (0.280 +/- 0.015) than in pretreated group (0.341 +/- 0.018, P less than 0.05). Lipid peroxide (LPO) in liver homogenates and serum were 1.86 +/- 0.43 n mol MDA/mg pr. and 12.26 +/- 0.84 n mol MDA/ml respectively in model group, whereas in pretreated group they gave a much lower value (1.19 +/- 0.12 and 6.55 +/- 2.97) respectively. Those data showed very significant difference between two groups (P less than 0.01). All of the above indices of pretreated group yielded values close to those of normal control group. The results of experimental study in vitro were identical to those of experimental study in vivo. These experimental studies suggested that RDQ provide antagonistic effect on endotoxin induced damage of lysosomes and mitochondria.